Biological explanation: Dopamine hypothesis

what is the original hypothesis?

positive sympotms of SZ are caused by an excess of dopamine

what do SZ have an excess of?

D2 receptors on receiving neurons

what does it mean if there are more D2 receptors?

more dopamine binding and more neurons firing

what was the evidence for the orignal hypothesis?

drug treatments

what are amphetamines?

dopamine agonist - they stimulate nerve cells containing dopamine

what happens if an individual is exposed to large quantities of of amphetamines?

develop SZ like symptoms

what are anti-pyschotic drugs?

block dopamine receptors

how do antipyschotics support the dopamine explaination?

they reduce SZ symptoms

who proposed the revised hypothesis?

Davis and Khan

what did Davis and Khan propose?

postive symptoms of SZ are a result from the excess dopamine in the subcortical areas of the brain - mesolimbic pathway

negative symptoms and cognitive symptoms are a result of dopamine deficits in the prefrontal cortex - mesocortical pathway

what did Patel et al find?

used PET scans of SZ and normal individuals and found lower levels of dopamine in the prefrontal cortex of SZ compared to controls

what does patel et al support?

revised hypothesis

what is the evaluation of the dopmaine hypothesis?

• success of treatments which block dopmaine receptors

• direction of causality

• reductionist and oversimplistic

what does it suggest if drugs reduce symptoms?

dopamine is an important factor in sympotms

what did crossley et al find?

a meta analysis that medication typically leads to a significant reduction in SZ synptoms

what do neuroleptic drugs do?

block dopmaine fiarly quickly but fail to reduce symptoms of SZ for days or weeks

what is puzzling about neuroleptic drugs?

puzzling if high levels of dopamine are responsible for maintaining the symptoms

what is treatment aetiology fallacy?

the success of treatments which block dopamine receptors doesnt mean that dopamine caused the condition in the first place

what is evidence for the dopmaine hypothesis?

mostly correlational - therefore we dont know the direction of causes

what confounding variables could affect the correlation?

stimulants

dopamine release from sources

what stimulants are confounding varibales?

cocaine and amphetamines affect dopamine levels but also other nuerotransmitter levels

what are other dopamine releases from sources?

stress and smoking

which are ignored

how is the dopmaine hypothesis reductionist and oversimplistic?

new anti-SZ drugs like clozapine work by affecting other neurotransmitters such a serotonin

what are neural correlates of SZ?

structural or functional brain features which are correlated aspects of SZ

what are the 2 examples of neural correlates?

• mesolimbic and mesocortical pathways associated with revised and dopamine hypothesis

• reduced neural communication between brocas and wernickes area may result in auditory hallucinations

what is supporting evidence for neural correlates?

ford et al

what did ford et al do?

• 7 healthy men anf 7 male SZ patients

• used erp to measure activities in temporal lobes where sounds are percieved (auditory cortex and wrenickles area)

• when listening to own spoken works and recording of played back speech

what were the results of ford et al?

• controls showed reduction in activity for their own spoken words than for played back speech

• SZ showed no such reduction

• ford later found that the disconnect between frontal and temporal areas was larger in patients prone to auditory hallucinations

what are the conclusions of ford et al?

reduced fronto-temporal communication may contribute to the misattribution of inner thoughts to external voices in SZ

what is the evaluation for neural correlates?

implications for treatment

what does early detection of poor frontotemporal communication and intervention mean?

can prevent the develop of the disorder

what does poor frontotemporal communication suggest about the dopamine hypothesis?

not a full explaination of SZ